The present research has demonstrated that prenatal stress will impair male copulatory behavior and enhance female lordotic behavior in male rats without inducing detectable modifications of reproductive morphology or physiology. Females are not affected. Neonatal stress has no effect on either sex. It is postulated that prenatal stress reduces the amount of androgen released by the fetal testes. Since androgen is needed during fetal development to organize the sexual behavior patterns characteristic of normal males, stress-induced attenuation of androgen will result in feminization and demasculinization of behavior. It is the objective of this proposal to extend the generality of this syndrome to species other than the rat and to stressors other than restraint. Also a more detailed appraisal of the nature of the deficit in ejaculatory behavior will be made through adult androgen treatment, intracranial implantation of testosterone propionate, and exposure to further stress in adulthood. Most importantly, we propose to investigate the nature of the hormonal mechanisms operating in both the mother and fetus to induce behavioral modifications under conditions of stress. These experiments are designed to (1) ascertain which hormone(s) are passed across the placental barrier to signal the existence of external stressors to the fetuses sheltered within the uterus, and (2) to directly measure the relative amounts of gonadal and gonadotrophic hormones contained in the plasma of control and stressed fetal males by means of radioimmunoassay. Finally, the effect of stressing the lactating mother on the process of sexual behavior differentiation of her suckling male offspring will be assessed.